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AHA- Nov 12, 2005 , Dallas
P.K.Shah, MD
Director of Cardiology and Atherosclerosis Research Center,
Cedars-Sinai Medical Center,
Professor of Medicine,
David Geffen School of Medicine at UCLA
Los Angeles, California
Imperative to Detect Subclinical Atherosclerosis
Aeha -aha symposium-nov-2005-short
Coronary Artery Disease
4 out of every 10 individuals who develop
a heart attack or sudden death from
coronary artery disease
have no prior warning or symptoms
CVD Risk Assessment in Asymptomatic Normal Subjects
Limitations of the Traditional Approach
PKS- CSMC
*One or more “Risk Factor” Accounts for 80-90% of
CHD Events
*Therefore Risk Factors can Predict most CHD Events
CVD Risk Assessment in Asymptomatic Normal Subjects
Limitations of the Traditional Approach
PKS- CSMC
0
10
20
30
40
50
60
70
80
90
100
Death Death/MI
% with > 1 Risk Factors
No Death/MINo Death
men
women
Pathophysiologic Paradigm in AtherosclerosisPathophysiologic Paradigm in Atherosclerosis
Oxidant StressOxidant Stress
Inflammatory Gene ActivationInflammatory Gene Activation
AtherosclerosisAtherosclerosis
Inflammatory Cell Recruitment/ActivationInflammatory Cell Recruitment/Activation
Modified LDL
Other mechanisms
Other mechanisms
Othermechanisms
Other mechanisms
Plaque-disruption/ThrombosisPlaque-disruption/Thrombosis
Genes Genes
Price M and Shah PK: Harrison’s Textbook of Medicne Online 2002
LDL , HDL , Diabetes-IRS-Metabolic Synd , Hypertension , Genetics, Others
Lipoproteins
Entry into Subendothelial Space
Lipoprotein Binding and Retention
Lipoprotein Modification (oxidation)
Inflammatory Gene Induction
Inflammation
Immune Activation
Athero-prone sites
LDL with Reduced Binding Affinity to Subendothelial Matrix is Associated
With Reduced Atherosclerosis Despite Severe Hypercholesterolemia
Skalen K et al: Nature 417:750:2002
Defective LDL
Normal LDL
CSMC--PKS
0
2
4
6
8
10
12
0
1
2
3
4
5
6
7
MyD88 +/+ +/- -/-
Genotype Normal Partial Complete
Deficiency Absence
Cholesterol
(mg/dl) 943 913 760
Cholesterol
(mg/dl) 943 913 760
Genetic Ablation of Myeloid Differentiation Factor (MyD88) Reduces
Atherosclerosis and Plaque Inflammation in Apo E Null Mice Despite Hypercholesterolemia
P<0.01
P<0.01
% Macrophage Immunoreactivity% Aortic Surface with Plaque
Michelsen, Wong, Shah, Arditi : PNAS 2004
MyD88 +/+ +/- -/-
Genotype Normal Partial Complete
Deficiency Absence
+ Risk Factors
+ Disease
+ Events
Atherosclerosis
And/or
(Pre-atherosclerosis)
Impaired Flow
Dynamics
Increased Stiffness
Disease Activity
(Biomarkers,
Plaque Phenotype)
Vaso-occlusive Clinical Events
*EBCT
*IMT
*MRI
Function
Stress Test
Endothelial
Function*CRP,LP-PLA2
*Gene SNP , Proteomics
*Plaque Composition
CVD Risk Assessment: A Different Paradigm
Traditional Risk Factor Based Disease Modification
Imaging for Identification of Subclinical Atherosclerosis
EBCT-MSCT, Carotid IMT, MRI
Non-invasive Assessment of Vascular Function
BART, ABI, Compliance , Stress Test
Markers for Disease Activity
Inflammatory and other Biomarkers
PKS- CSMC
Aeha -aha symposium-nov-2005-short

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Aeha -aha symposium-nov-2005-short

  • 1. AHA- Nov 12, 2005 , Dallas P.K.Shah, MD Director of Cardiology and Atherosclerosis Research Center, Cedars-Sinai Medical Center, Professor of Medicine, David Geffen School of Medicine at UCLA Los Angeles, California Imperative to Detect Subclinical Atherosclerosis
  • 3. Coronary Artery Disease 4 out of every 10 individuals who develop a heart attack or sudden death from coronary artery disease have no prior warning or symptoms
  • 4. CVD Risk Assessment in Asymptomatic Normal Subjects Limitations of the Traditional Approach PKS- CSMC *One or more “Risk Factor” Accounts for 80-90% of CHD Events *Therefore Risk Factors can Predict most CHD Events
  • 5. CVD Risk Assessment in Asymptomatic Normal Subjects Limitations of the Traditional Approach PKS- CSMC 0 10 20 30 40 50 60 70 80 90 100 Death Death/MI % with > 1 Risk Factors No Death/MINo Death men women
  • 6. Pathophysiologic Paradigm in AtherosclerosisPathophysiologic Paradigm in Atherosclerosis Oxidant StressOxidant Stress Inflammatory Gene ActivationInflammatory Gene Activation AtherosclerosisAtherosclerosis Inflammatory Cell Recruitment/ActivationInflammatory Cell Recruitment/Activation Modified LDL Other mechanisms Other mechanisms Othermechanisms Other mechanisms Plaque-disruption/ThrombosisPlaque-disruption/Thrombosis Genes Genes Price M and Shah PK: Harrison’s Textbook of Medicne Online 2002 LDL , HDL , Diabetes-IRS-Metabolic Synd , Hypertension , Genetics, Others
  • 7. Lipoproteins Entry into Subendothelial Space Lipoprotein Binding and Retention Lipoprotein Modification (oxidation) Inflammatory Gene Induction Inflammation Immune Activation Athero-prone sites
  • 8. LDL with Reduced Binding Affinity to Subendothelial Matrix is Associated With Reduced Atherosclerosis Despite Severe Hypercholesterolemia Skalen K et al: Nature 417:750:2002 Defective LDL Normal LDL
  • 9. CSMC--PKS 0 2 4 6 8 10 12 0 1 2 3 4 5 6 7 MyD88 +/+ +/- -/- Genotype Normal Partial Complete Deficiency Absence Cholesterol (mg/dl) 943 913 760 Cholesterol (mg/dl) 943 913 760 Genetic Ablation of Myeloid Differentiation Factor (MyD88) Reduces Atherosclerosis and Plaque Inflammation in Apo E Null Mice Despite Hypercholesterolemia P<0.01 P<0.01 % Macrophage Immunoreactivity% Aortic Surface with Plaque Michelsen, Wong, Shah, Arditi : PNAS 2004 MyD88 +/+ +/- -/- Genotype Normal Partial Complete Deficiency Absence
  • 10. + Risk Factors + Disease + Events
  • 11. Atherosclerosis And/or (Pre-atherosclerosis) Impaired Flow Dynamics Increased Stiffness Disease Activity (Biomarkers, Plaque Phenotype) Vaso-occlusive Clinical Events *EBCT *IMT *MRI Function Stress Test Endothelial Function*CRP,LP-PLA2 *Gene SNP , Proteomics *Plaque Composition
  • 12. CVD Risk Assessment: A Different Paradigm Traditional Risk Factor Based Disease Modification Imaging for Identification of Subclinical Atherosclerosis EBCT-MSCT, Carotid IMT, MRI Non-invasive Assessment of Vascular Function BART, ABI, Compliance , Stress Test Markers for Disease Activity Inflammatory and other Biomarkers PKS- CSMC